Fungal surfaces undergo profound changes during morphogenesis that modify host responses. For example, inhaled spores or conidia of Rhizopus or Aspergillus lose their surface hydrophobic outer layers, initially swell, and then germinate to form mycelia that may invade tissues. These various fungal forms not only elicit differing response from host phagocytic cells but also differ in their susceptibilities to cellular microbicidal mechanisms. In addition, studies comparing neutrophil activation responses to opsonized and unopsonized Candida hyphae indicate that the presence or absence of antibody or complement on fungal surfaces determines distinct patterns of the early responses of neutrophils to stimulation, such as membrane depolarization, cytosolic increase in calcium, and phosphoinositide turnover. These initial events in the neutrophil activation sequence are followed by release of both fungicidal granule constituents and oxidants from the respiratory burst. The quantity and specificity of delivery of these toxic neutrophil products ultimately determine the relative efficiency of fungicidal activity versus inflammatory cytotoxicity to host cells.